We hope to focus on the role of "mineralocorticoid" steroids in hypertension. A few individuals with high blood pressure have elevations of the mineralocorticoids aldosterone and (or) deoxycorticosterone. Clinical features in certain other patients with hypertension suggest that excess mineralocorticoids are present; but the known mineralocorticoids appear to be normal. Thus, it is possible that hypertension in these cases is due to elevated mineralocorticoid activity due to: undetected steroids; a combination of steroids which individually measured are normal; or an increase in free steroids because of decreased plasma binding. In the proposed studies, we hope to study this question by using specific receptors which appear to mediate actions of the known mineralocorticoid hormones. We hope to refine a technique utilizing these receptors in kidney slices which are incubated with plasma and radioactive aldosterone. In this way, any plasma sample which contains elevations of free steroids, alone or in combination, which can act as mineralocorticoids through these receptors will have an elevated capacity to bind to the receptor and thus to inhibit binding of radioactive aldosterone. We hope to study plasma from the various patients suspected of having "mineralocorticoid" hypertension. We also hope to study plasma binding, the receptor binding affinities, and the concentrations of various steroids with possible mineralocorticoid activity in plasma to bind to the receptors. These relations can then be used in a predictive sense, where the steroids are measured individually, to determine the extent to which elevations are capable of significant occupancy of the mineralocorticoid receptors and thus of eliciting mineralocorticoid actions. We feel that such information will help to understand the extent to which the mineralocorticoid steroids contribute to the pathogenesis of hypertensive cardiovascular disease.